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NUE 325: Pathopharm I > Pharamcology Principles > Flashcards

Pharamcology Principles Flashcards

1
Q

Three phases of drug action

A

1: pharmaceutic phase
2: pharmacokinetics phase
3: pharmacodynamics phase

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2
Q

Pharmaceutical phase

A

The breakdown of tablets into smaller and smaller particles that can be absorbed in the blood
- only for PO drugs
- must occur to be absorbed

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3
Q

Pharmacokinetics phase

A

What happens to the drug in the body after it has been broken down and absorbed
- drug absorbed by SI, enters blood and transported to sites of action
- four processes: absorption, distribution, metabolism/biotransformation, excretion

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4
Q

Drugs and phospholipid bilayer

A

Cell membranes are composed of lipids, so only lipid soluble compounds can easily migrate across
- we make drugs lipid soluble
- water soluble drugs are transported by membrane channels or pores

absorption

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5
Q

First pass effect

A

Refers to the metabolism of the drug in the liver before entering systemic circulation
-liver breaks down certain percentage of drug into bioavailable form (active) —the amount of drug left after first pass
- PO: bioavailability varies
-IV: bioavailability is 100%

absorption

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6
Q

Routes of absorption

A

1) enteral
2) prenteral
3) topical

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7
Q

Enteral absorption

A

GI tract (oral/gastric mucosa, SI, rectum)
- EC (enteric coated, breakdown and absorption in SI) (first pass)
- PO (breakdown in stomach, absorbed in SI (first pass effect
- SL, buccal, rectal (highly vascular. So no first pass)

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8
Q

Parenteral absorption

A

SQ, IM, IV, intrathecal (spinal cord), epidural (dural space)
- IV is fastest
- none are first pass

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9
Q

Topical absorption

A

Application of meds to body surfaces
- eyes, skin, ears, nose, lungs
- slower onset, no first pass bc localized

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10
Q

Distribution in pharmacokinetics phase

A

The movement of drug through the body and the process of drugs leaving blood and entering site of action
- depends largely on adequacy of blood circulation bc drug has easier time getting to site

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11
Q

Examples of disruption of distribution in pharmacokinetics phase

A
  • peripheral vascular disease
  • abscesses
  • tumors
  • drugs can’t get to site of action to heal *
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12
Q

Blood brain barrier (BBB)

A

Tight junctions of the capillary walls endothelial cells
- prevent easy passage of drugs
- drugs need transport system or extremely lipid soluble
- alcohol, glucose can pass

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13
Q

protein binding effect

A

Purpose: temporarily store drug molecules so they are available for longer periods of time which helps maintain steady free drug conc
- reversible process
- drugs must be unbound to exert effect
- albumin is primary plasma protein that binds drugs
drugs can be high protein bound or low

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14
Q

Hypoalbuminemia

A

Low protein levels (albumin)
- allows for increase in free drugs which risk possibility of overdose/toxicity
- ex: warfarin

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15
Q

Metabolism of pharmacokinetics

A

Biotransformation — drugs are inactivated in liver into metabolites
- lipid soluble to water soluble
- performed by cytochrome P-450

importance: if liver is not working, drugs are not inactivated, risk toxicity

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16
Q

Cytochrome P-450 (aka CYP450)

A

Group of isoenzymes that metabolize drugs
- metabolize 1/2 of all drugs
- drug - drug interactions can occur when taken concurrently

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17
Q

Types of CYP450

A
  • substrate: drug uses CYP450 for metabolism, converts active forms
  • inducer: speeds of CYP450 (increases breakdown), decreases drug and therapeutic effect
  • inhibitor: inhibits CYP450 (decreases breakdown), increases drug and risk toxicity
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18
Q

Excretion of pharmacokinetics

A

Elimination of drugs from the body by the kidneys
- generally hydrophilic (water soluble) drugs
- some drugs are reabsorbed (renal tubules)

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19
Q

Effects of kidney disease on excretion

A

Drugs are not excreted and can build up causing toxicity
- check with renal labs (blood urea N, creatinine)
- glomerular filtration rate: best measure of kidney function (related to free drug conc in plasma)

20
Q

Half life:

A

Serum half-life: time required for serum conc to decrease by 50%
- takes 5 half lives to be 97% eliminated
- about 4-5 half lives for steady state to occur which is when the drug = amount metabolized/excreted
- dictates dosage, frequency

21
Q

Around the clock dosing (ATC)

A

Goal to maintain 50% drug conc in body
- used to treat chronic pain
- PRN for breakthrough pain

22
Q

Onset

A

Time it takes for drugs to elicit therapeutic response

23
Q

Peak

A

Time it takes for drugs to reach max therapeutic effect

24
Q

duration

A

Time drug conc is sufficient to elicit a therapeutic response

25
Q

Pharmacodynamics

A

What the drug does in the body like increase, decrease, replace, inhibit, destroy, protect, or irritate to CREATE A RESPONSE
- drugs exert multiple effects on body (some desired some not)
- ex: slide 64 metaproterenol

26
Q

Importance of receptors

A

Receptors are found on cell membrane surface and composed of proteins
- chemical (drugs) will bind to create drug-receptor complex that will produce effects
- categorized as agonist/antagonist
some drugs don’t need receptors and act with simple physical/chemical interactions

27
Q

Agonist

A

Drug with ability to initiate desired therapeutic effect when binding
- occupy receptor and activate
- ex: drug binds causing vasodilation to lower peripheral vascular resistance

28
Q

Antagonist

A

Drug that binds and prevent/block/inhibits other ligands from binding so not response is activated
- occupy receptor and block
- ex: Zantac blocks release of gastric acid

29
Q

Therapeutic index

A

Amount of drug needed in the body to have an effect and not be at toxic levels
- measures relative safety of drug

30
Q

Narrow therapeutic index

A

Ratios with lowest conc of drug at which clinical toxicity can occur

31
Q

Black box warning

A

FDA warning that drug is especially dangerous
- strongest safety warning and still remain in market
- must have warning on package insert, product label, advertising

32
Q

Processes to prevent med errors

A

-restrict high alert meds and med routes
- drug differentiation (using tall-man)
- computerized admin
- pt info accessible
- standardize and simplify
- apply reminders
- include pt in therapy
- don’t use trailing zeros
- use leading zeros

33
Q

High alert medications

A

Meds most likely to cause serious harm
- insulin, heparin, opioids, injectable potassium chloride, neuromuscular blocking agents, chemo drugs

34
Q

Drug interactions

A

-drug- drug
-drug- food
-drug- herb
-drug- disease

35
Q

Ways nurse can minimize drug interactions

A

-decrease number of drugs
-through drug history
-extra vigilant monitoring narrow therapeutic index

36
Q

Drug interactions that increase therapeutic effect

A
  • additive effects
  • synergism/potentiation
  • activation
  • displacement
37
Q

Additive effects

A

2 drugs with similar MOA that make stronger effect

38
Q

Synergism/potentiation

A

2 drugs w diff MOA but combine have greater effect than either drug alone

39
Q

Activation

A

Drug metabolizing enzyme in liver that decrease CYP450, so decrease metabolism rate
-purposely altering metabolism

40
Q

Displacement

A

Displacement of one drug from plasma protein binding sites by a second drug increases effect of displaced drug
- how much drug is available due to protein binding

41
Q

Drug interactions that decrease therapeutic effects

A

-antidote
-decrease intestinal absorption
- activation

42
Q

Antidote

A

Given to antagonize toxic effects of another drug

43
Q

Decrease intestinal absorption

A

In relation to PO meds, does pt have healthy intestines to break down drugs and absorb

44
Q

Activation

A

Activating drug metabolizing enzymes in the liver to induce
- increase metabolism rate (quicker out of body)
- CYP450 system

45
Q

Consideration for older adults and pharmacokinetics

A
  • hepatic changes: drugs metabolize slower
  • gastrointestinal changes: decrease absorption of oral drugs
  • cardiac and circulatory changes: impaired circulation means decreased distribution of drugs
  • renal changes: drugs are excreted less completely

NUE 325: Pathopharm I (23 decks)

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